This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Emotional responses to stress are linked with immune and inflammatory changes, such as changes to inflammatory cytokine profiles, and new research suggests that such changes are implicated in the aggravation of long-term pain. Our overall objective is to examine the impact of emotion on pain and inflammatory responses to pain, as well as the degree to which inflammation and other physiological factors explain associations between emotion, perceived stress, and pain. This will be examined among individuals with rheumatoid arthritis, for whom additional strategies to manage pain are greatly needed and for whom emotional regulation may be particularly important. During each of 3 proposed "emotion" visits, spaced about 1 month apart, 40 individuals will complete emotion-focusing exercises to elicit either anger, depressed mood, or positive emotion;these visits will be contrasted with a baseline control visit during which emotion is not elicited. During each visit, blood will be drawn at baseline and just before, during, and 30 minutes after a pain threshold test. Blood will be assayed for C-reactive protein (baseline only), and proinflammatory cytokines TNF-a, IL-1, IL-6, anti-inflammatory cytokine interleukin-10 (IL-10), cortisol, and catecholamines. We expect that (1) both state anger and negative mood will increase RA pain severity and, in response to acute pain, will increase cortisol and proinflammatory cytokine responses. Positive emotion will have the opposite effects;(2) Cytokine changes will account for the effects of state emotion on both pain severity from RA and pain threshold.